Axons impulse transmission along

Ion transport is central to nerve impulse transmission both along the axon and at the synapse and many neurotoxicants elicit effects by interfering with the normal transport of these ions (Figure 11.6). The action potential of an axon is maintained by the high concentration of sodium on the outside of the cell as compared to the low concentration inside. Active transporters of sodium (Na+K+ ATPases) that actively transport sodium out of the cell establish this action potential. One action of the insecticide DDT resulting in its acute toxicity is the inhibition of these Na+K+ ATPases resulting in the inability of the nerve to establish an action potential. Pyrethroid insecticides also elicit neurotoxicity through this mechanism. DDT also inhibits Ca2+Mg2+ ATPases, which are important to neuronal repolarization and the cessation of impulse transmission across synapses. 

When a nerve impulse reaches the synaptic knob the neurotransmitter is ejected into the synaptic cleft and serves as a stimulus to the next adjacent neuron. The vast majority of all impulses transmitted occur at the synaptic gaps, although recent research indicates that chemical transmission can occur at other points along the axon. Many neurological diseases and psychiatric disorders result from a disturbance or alteration of synaptic activity. Drugs such as tranquilizers, anesthetics, nicotine, and caffeine target the synapse and can cause an alteration of impulse transmission. 

A nerve impulse propagated along the axon must be transmitted across the synaptic cleft to be further propagated. An impulse does not come alone, but in a train of impulses. Because impulse transmission in an axon is an all-or-nothing phenomenon, it is the frequency and not the amplitude of each impulse that determines the strength of the signal. The mechanism, now fairly well understood, is described briefly. 

We have already noted above that in analyzing excitable systems one has, more often than not, to deal with a parabolic equation with a nonlinear source. In this section we will concern ourselves with an excitable medium of a different type, where the signals are transmitted in the neuron network not by the local currents but by the nervous impulses traveling along the axons. The propagation speed of the activity wave will, if this transmission mode is possible at all, depend not only on the signal transmission speed but also on the other characteristics of nerve cells such as cell body capacitance, conductance, etc. 

The idea that signals are transmitted along the nerve channels as an electric current had arisen as early as the middle of the nineteenth century. Yet even the first measurements performed by H. Helmholtz showed that the transmission speed is about lOm/s (i.e., much slower than electric current flow in conductors). It is known today that the propagation of nerve impulses along the axons of nerve cells (which in humans are as long as 1.5m) is associated with an excitation of the axon s outer membrane. 

The observations described in the following chapter show that Ch. E. is highly concentrated everyivhere at the neuronal surface. There is only a quantitative difference between axon and synapse, the enzj me concentration being higher at the synapse where the neuronal surface increases due to the extensive end-arborization. This is consistent with the view that ACh may have the same role in the transmission of the nerve impulse along the axon as across the. synapse and that the difference may be only a quantitative one. 

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